Over the last decade several approaches to the biological role of nitric oxide (NO) have been made. The synthesis of NO, which is catalysed by specialized NO synthases using L-arginine as a substrate, has now been shown to take place in many cell types (Nathan C., FASEB J. 6 (1992) 3051-64). The NO synthase exists in several isotypes that can be divided into two major classes: constitutive and inducible. The constitutive isotypes have been described in endothelial cells (Moncada S. et al., Pharmacol. Rev. 43 (1991) 109-42) and for instance in parasympathetic vasodilator nerves (Kummer W. et al., Neuroreport 3 (1992) 653-55). The inducible isotypes are found, after activation, in macrophages, neutrophils, endothelium, vascular smooth muscle (Moncada S. et al., Pharmacol. Rev. 43 (1991) 109-42) and even epithelium in the airways of asthmatic subjects (Springall et al., Am. Rev. Resp. Dis. 147 (1993) A515). The production of NO has so far been difficult to measure directly in vivo, although increases in the end-products nitrite and nitrate in plasma and urine can be used in some cases (Archer S., FASEB J. 7 (1992) 349-360). Recently, it was shown, however, that NO can be found in parts per billion (p.p.b.) levels in exhaled air of experimental animals and humans (Gustafsson L. E. et al., Biochem. Biophys. Res. Commun. 181 (1992) 852-7). Gustafsson et al have measured NO levels either by connecting a chemiluminescence detector to the exhaled air or by bubbling the exhaled air through a solution in which NO was chemically trapped. The human experiments appear to have been performed on one single individual who was allowed to inhale through the nose and exhale through the mouth. The relatively high NO level Gustafsson et al. have obtained compared to ours might be explained by passage of NO into the inhaled air when it passes through the nose. In a later publication Persson M. G. and Gustafsson L. E. have reported that ethanol intake will reduce NO formation as measured in exhaled air of rabbits (Eur. J. Pharmacol. 224 (1992) 99-100). Gustafsson L. E. himself has also suggested that measured NO levels in exhaled air may be used to check lung function (WO-A-9305709 and SE-91032433). The works of Gustafsson L. E. et al appears to be the closest prior art. During the priority year, data on increased levels of NO in exhaled air of asthmatic patients and decreased levels smokers have been published (Alving K. et al., Eur. Resp. J. 6 (October, 1993) 1368-70; Hamid Q. et al., Lancet 342 (December 1993) 1510-13; Karithonov S. A. et al., Lancet 343 (January 1994) 133-35; and Persson M. G et al., Lancet 343 (January 1994) 146-7.